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. Author manuscript; available in PMC: 2014 Apr 1.
Published in final edited form as: Nat Rev Neurosci. 2013 Mar 13;14(4):265–277. doi: 10.1038/nrn3468

Figure 5. Proposed role of aquaporin 4 in the pathogenesis of neuromyelitis optica.

Figure 5

a | Circulating aquaporin 4 (AQP4)-specific immunoglobulin G (IgG) enters the CNS and binds to AQP4 on astrocyte foot processes. Complement is activated via the classical pathway with deposition of C5b–C9 complexes in astrocyte cell plasma membranes. b | Activated complement components attract peripheral leukocytes (primarily neutrophils and eosinophils) into the lesion, which degranulate, causing astrocyte death. c | Chemokines (from dying astrocytes and activated leukocytes) attract macrophages, causing death of oligodendrocytes and neurons. d | Microglia enter the lesion as well as reactive astrocytes, which express AQP4 and form a glial scar. The lesion core is necrotic with a macrophage infiltrate.